Breast cancer is the most common tumor and ranks top in causes of woman tumor-related deaths worldwide [1]. Despite efforts to improve the survival rate of patients, there are still problems related with breast cancer treatment including metastasis and drug resistance [2, 3]. Tumors consist of cancer stem cells (CSCs) and non-tumorigenic cells that form tumor mass [4]. The CSCs are considered as a cause of tumor, tumor metastasis, drug resistance, and tumor recurrence [5]. In particular, breast cancer stem cells (BCSCs) has a characteristic of stem cells and are characterized by expression of cell surface markers CD44+/CD24− [6]. Different miRNAs are involved in the formation and regulation of human breast cancer stem cells [7], and according to preceding studies, ectopic expression of miR-34c inhibits migration of epithelial-mesenchymal cells and reduces self-renewal capacity in human breast cancer stem cells [8].
Serine/threonine-protein kinase D1 (PKD1) acts as diacylglycerol and protein kinase C (PKC) effectors to mediate stimulatory activity [9]. PKD/PKCμ related cellular processes were activated by two phosphorylations through PKC-dependent phosphorylation (Ser744/Ser748) and PKC-independent autophosphorylation (Ser910) [10-13]. Therefore, PRKD1 is considered as a major regulator in many cellular processes including a NF-kB signaling pathway, cell cycle progression, DNA synthesis, and regulation of other pathogenic conditions [14-16].
In breast cancer, microRNAs regulate apoptosis, tumor formation and angiogenesis. A major regulator of tumor suppression, miR-34, is a direct transcriptional target for a tumor inhibitor p53, and a miR-34a promoter region includes a p53-binding site [17]. In breast cancer studies, the miR-34a plays a role in inhibiting cell survival by up-regulating p53 after irradiation after DNA damage [18]. In addition, the miR-34a promoted tumor apoptosis by targeting Bcl-2 and SIRT1 [19]. Therefore, the miR-34a is associated with a target that induces breast cancer.